Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients

Background: Various human cardiovascular pathophysiological conditions associate aberrant expression of microRNAs (miRNAs) and circulating miRNAs are emerging as promising biomarkers. In mice, myocardial miR-21 overexpression is related to cardiac fibrosis elicited by pressure overload. This study w...

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Autores: Villar Ramos, Ana Victoria, García López, Raquel, Merino Fernández, David, Llano Cardenal, Miguel, Cobo Belaustegui, Manuel, Montalvo Silva, Cecilia de, Martín Durán, Rafael, Hurlé González, María Amor, Nistal Herrera, Juan Francisco|||0000-0002-4152-7621
Tipo de recurso: artículo
Fecha de publicación:2012
País:España
Institución:Universidad de Cantabria (UC)
Repositorio:UCrea Repositorio Abierto de la Universidad de Cantabria
Idioma:inglés
OAI Identifier:oai:repositorio.unican.es:10902/1127
Acceso en línea:http://hdl.handle.net/10902/1127
Access Level:acceso abierto
Palabra clave:Aortic stenosis
Myocardial fibrosis
MicroRNA
Plasma miR-21
TGF-β signaling
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spelling Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patientsVillar Ramos, Ana VictoriaGarcía López, RaquelMerino Fernández, DavidLlano Cardenal, MiguelCobo Belaustegui, ManuelMontalvo Silva, Cecilia deMartín Durán, RafaelHurlé González, María AmorNistal Herrera, Juan Francisco|||0000-0002-4152-7621Aortic stenosisMyocardial fibrosisMicroRNAPlasma miR-21TGF-β signalingBackground: Various human cardiovascular pathophysiological conditions associate aberrant expression of microRNAs (miRNAs) and circulating miRNAs are emerging as promising biomarkers. In mice, myocardial miR-21 overexpression is related to cardiac fibrosis elicited by pressure overload. This study was designed to determine the role of myocardial and plasmatic miR-21 in the maladaptive remodeling of the extracellular matrix induced by pressure overload in aortic stenosis (AS) patients and the clinical value of miR-21 as a biomarker for pathological myocardial fibrosis. Methods: In left ventricular biopsies from 75 AS patients and 32 surgical controls, we quantified the myocardial transcript levels of miR-21, miR-21-targets and ECM- and TGF-β-signaling-related elements. miR-21 plasma levels were determined in 25 healthy volunteers and in AS patients. In situ hybridization of miR-21 wasperformed in myocardial sections. Results: The myocardial and plasma levels of miR-21 were significantly higher in the AS patients compared with controls and correlated directly with the echocardiographic mean transvalvular gradients. miR-21 overexpression was confined to interstitial cells and absent in cardiomyocytes. Using bootstrap validated multiple linear regression, the variance in myocardial collagen expression was predicted by myocardial miR-21 (70% of collagen variance) or plasma miR-21 (52% of collagen variance), together with the miR-21 targets RECK and PDCD4, and effectors of TGF-β signaling. Conclusions: Our results support the role of miR-21 as a regulator of the fibrotic process that occurs in response to pressure overload in AS patients and underscore the value of circulating miR-21 as a biomarker for myocardial fibrosis.This work was supported by the Instituto de Salud Carlos III [PS09/01097], Ministerio de Ciencia e Innovación (SAF2010-16894), Fundación Marqués de Valdecilla Universidad de Cantabria [FMV-UC 09/01], and Instituto de Formación e Investigación Marqués de Valdecilla [FMV-API 10/20]ElsevierUniversidad de Cantabria20122012-08-08journal articlehttp://purl.org/coar/resource_type/c_6501NAhttp://purl.org/coar/version/c_be7fb7dd8ff6fe43info:eu-repo/semantics/articlehttp://hdl.handle.net/10902/1127International Journal of Cardiology, 2013, 167(6), 2875-81reponame:UCrea Repositorio Abierto de la Universidad de Cantabriainstname:Universidad de Cantabria (UC)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:repositorio.unican.es:10902/11272026-06-02T12:39:31Z
dc.title.none.fl_str_mv Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
title Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
spellingShingle Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
Villar Ramos, Ana Victoria
Aortic stenosis
Myocardial fibrosis
MicroRNA
Plasma miR-21
TGF-β signaling
title_short Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
title_full Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
title_fullStr Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
title_full_unstemmed Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
title_sort Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients
dc.creator.none.fl_str_mv Villar Ramos, Ana Victoria
García López, Raquel
Merino Fernández, David
Llano Cardenal, Miguel
Cobo Belaustegui, Manuel
Montalvo Silva, Cecilia de
Martín Durán, Rafael
Hurlé González, María Amor
Nistal Herrera, Juan Francisco|||0000-0002-4152-7621
author Villar Ramos, Ana Victoria
author_facet Villar Ramos, Ana Victoria
García López, Raquel
Merino Fernández, David
Llano Cardenal, Miguel
Cobo Belaustegui, Manuel
Montalvo Silva, Cecilia de
Martín Durán, Rafael
Hurlé González, María Amor
Nistal Herrera, Juan Francisco|||0000-0002-4152-7621
author_role author
author2 García López, Raquel
Merino Fernández, David
Llano Cardenal, Miguel
Cobo Belaustegui, Manuel
Montalvo Silva, Cecilia de
Martín Durán, Rafael
Hurlé González, María Amor
Nistal Herrera, Juan Francisco|||0000-0002-4152-7621
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad de Cantabria
dc.subject.none.fl_str_mv Aortic stenosis
Myocardial fibrosis
MicroRNA
Plasma miR-21
TGF-β signaling
topic Aortic stenosis
Myocardial fibrosis
MicroRNA
Plasma miR-21
TGF-β signaling
description Background: Various human cardiovascular pathophysiological conditions associate aberrant expression of microRNAs (miRNAs) and circulating miRNAs are emerging as promising biomarkers. In mice, myocardial miR-21 overexpression is related to cardiac fibrosis elicited by pressure overload. This study was designed to determine the role of myocardial and plasmatic miR-21 in the maladaptive remodeling of the extracellular matrix induced by pressure overload in aortic stenosis (AS) patients and the clinical value of miR-21 as a biomarker for pathological myocardial fibrosis. Methods: In left ventricular biopsies from 75 AS patients and 32 surgical controls, we quantified the myocardial transcript levels of miR-21, miR-21-targets and ECM- and TGF-β-signaling-related elements. miR-21 plasma levels were determined in 25 healthy volunteers and in AS patients. In situ hybridization of miR-21 wasperformed in myocardial sections. Results: The myocardial and plasma levels of miR-21 were significantly higher in the AS patients compared with controls and correlated directly with the echocardiographic mean transvalvular gradients. miR-21 overexpression was confined to interstitial cells and absent in cardiomyocytes. Using bootstrap validated multiple linear regression, the variance in myocardial collagen expression was predicted by myocardial miR-21 (70% of collagen variance) or plasma miR-21 (52% of collagen variance), together with the miR-21 targets RECK and PDCD4, and effectors of TGF-β signaling. Conclusions: Our results support the role of miR-21 as a regulator of the fibrotic process that occurs in response to pressure overload in AS patients and underscore the value of circulating miR-21 as a biomarker for myocardial fibrosis.
publishDate 2012
dc.date.none.fl_str_mv 2012
2012-08-08
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
NA
http://purl.org/coar/version/c_be7fb7dd8ff6fe43
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10902/1127
url http://hdl.handle.net/10902/1127
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv International Journal of Cardiology, 2013, 167(6), 2875-81
reponame:UCrea Repositorio Abierto de la Universidad de Cantabria
instname:Universidad de Cantabria (UC)
instname_str Universidad de Cantabria (UC)
reponame_str UCrea Repositorio Abierto de la Universidad de Cantabria
collection UCrea Repositorio Abierto de la Universidad de Cantabria
repository.name.fl_str_mv
repository.mail.fl_str_mv
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